scholarly journals Seizures Caused by Exposure to Hyperbaric Oxygen in Rats Can Be Predicted by Early Changes in Electrodermal Activity

2022 ◽  
Vol 12 ◽  
Author(s):  
Hugo F. Posada-Quintero ◽  
Carol S. Landon ◽  
Nicole M. Stavitzski ◽  
Jay B. Dean ◽  
Ki H. Chon
Keyword(s):  
Nervous System ◽  
Hyperbaric Oxygen ◽  
Electrodermal Activity ◽  
Radio Telemetry ◽  
Core Body Temperature ◽  
Ambient Pressure ◽  
Oxygen Toxicity ◽  
Hyperbaric Chamber ◽  
Generalized Seizures ◽  
Animal Chamber

Hyperbaric oxygen (HBO2) is breathed during undersea operations and in hyperbaric medicine. However, breathing HBO2 by divers and patients increases the risk of central nervous system oxygen toxicity (CNS-OT), which ultimately manifests as sympathetic stimulation producing tachycardia and hypertension, hyperventilation, and ultimately generalized seizures and cardiogenic pulmonary edema. In this study, we have tested the hypothesis that changes in electrodermal activity (EDA), a measure of sympathetic nervous system activation, precedes seizures in rats breathing 5 atmospheres absolute (ATA) HBO2. Radio telemetry and a rodent tether apparatus were adapted for use inside a sealed hyperbaric chamber. The tethered rat was free to move inside a ventilated animal chamber that was flushed with air or 100% O2. The animal chamber and hyperbaric chamber (air) were pressurized in parallel at ~1 atmosphere/min. EDA activity was recorded simultaneously with cortical electroencephalogram (EEG) activity, core body temperature, and ambient pressure. We have captured the dynamics of EDA using time-varying spectral analysis of raw EDA (TVSymp), previously developed as a tool for sympathetic tone assessment in humans, adjusted to detect the dynamic changes of EDA in rats that occur prior to onset of CNS-OT seizures. The results show that a significant increase in the amplitude of TVSymp values derived from EDA recordings occurs on average (±SD) 1.9 ± 1.6 min before HBO2-induced seizures. These results, if corroborated in humans, support the use of changes in TVSymp activity as an early “physio-marker” of impending and potentially fatal seizures in divers and patients.

A potential early physiological marker for CNS oxygen toxicity: hyperoxic hyperpnea precedes seizure in unanesthetized rats breathing hyperbaric oxygen

2013 ◽  
Vol 114 (8) ◽  
pp. 1009-1020 ◽  
Author(s):  
Raffaele Pilla ◽  
Carol S. Landon ◽  
Jay B. Dean
Keyword(s):  
Hyperbaric Oxygen ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Phase 1 ◽  
Oxygen Toxicity ◽  
Sprague Dawley ◽  
Hyperbaric Chamber ◽  
Phase 3 ◽  
Sprague Dawley Rats ◽  
Animal Chamber

Hyperbaric oxygen (HBO2) stimulates presumptive central CO2-chemoreceptor neurons, increases minute ventilation (V̇min), decreases heart rate (HR) and, if breathed sufficiently long, produces central nervous system oxygen toxicity (CNS-OT; i.e., seizures). The risk of seizures when breathing HBO2 is variable between individuals and its onset is difficult to predict. We have tested the hypothesis that a predictable pattern of cardiorespiration precedes an impending seizure when breathing HBO2. To test this hypothesis, 27 adult male Sprague-Dawley rats were implanted with radiotelemetry transmitters to assess diaphragmatic/abdominal electromyogram, electrocardiogram, and electroencephalogram. Seven days after surgery, each rat was placed in a sealed, continuously ventilated animal chamber inside a hyperbaric chamber. Both chambers were pressurized in parallel using poikilocapnic 100% O2 (animal chamber) and air (hyperbaric chamber) to 4, 5, or 6 atmospheres absolute (ATA). Breathing 1 ATA O2 initially decreased V̇min and HR ( Phase 1 of the compound hyperoxic ventilatory response). With continued exposure to normobaric hyperoxia, however, V̇min began increasing toward the end of exposure in one-third of the animals tested. Breathing HBO2 induced an early transient increase in V̇min ( Phase 2) and HR during the chamber pressurization, followed by a second significant increase of V̇min ≤8 min prior to seizure ( Phase 3). HR, which subsequently decreased during sustained hyperoxia, showed no additional changes prior to seizure. We conclude that hyperoxic hyperpnea ( Phase 3 of the compound hyperoxic ventilatory response) is a predictor of an impending seizure while breathing poikilocapnic HBO2 at rest in unanesthetized rats.

Diving medicine

2010 ◽  
pp. 1416-1422
Author(s):  
D.M. Denison ◽  
M.A. Glover
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Partial Pressure ◽  
Ambient Pressure ◽  
Inert Gases ◽  
Gas Mixture ◽  
Generalized Seizures ◽  
Partial Pressures ◽  
Diving Medicine ◽  
The Central Nervous System

Diving remains the principal means of exploring and exploiting shallower underwater zones. Immersion and rapid increase in pressure with depth cause most problems unique to diving. Gas density, partial pressures, and solubility vary proportionately with ambient pressure. At elevated partial pressure, nitrogen becomes narcotic, as can other inert gases, and contaminants barely detectable at the surface can become toxic as their partial pressures rise with depth. Hyperoxia irritates the lungs and the central nervous system, and sometimes causing generalized seizures. A safe gas mixture at depth can become hypoxic as the partial pressure of oxygen decreases during the return to surface....

scholarly journals Humidity does not affect central nervous system oxygen toxicity

2001 ◽  
Vol 91 (3) ◽  
pp. 1327-1333 ◽  
Author(s):  
R. Arieli ◽  
Y. Moskovitz
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Water Vapor ◽  
Metabolic Rate ◽  
Hyperbaric Oxygen ◽  
Medical Therapy ◽  
Electrical Discharge ◽  
Oxygen Toxicity ◽  
Loss Of Consciousness ◽  
Hyperbaric Therapy

Central nervous system (CNS) oxygen toxicity can occur as convulsions and loss of consciousness when hyperbaric oxygen is breathed in diving and hyperbaric medical therapy. Lin and Jamieson ( J Appl Physiol 75: 1980–1983, 1993) reported that humidity in the inspired gas enhances CNS oxygen toxicity. Because alveolar gas is fully saturated with water vapor, we could not see a cause and effect and surmised that other factors, such as metabolic rate, might be involved. Rats were exposed to 507- and 608-kPa O2 in dry (31 or 14%) or humid (99%) atmosphere until the appearance of the first electrical discharge preceding the clinical convulsions. Each rat served as its own control. A thermoneutral temperature (28 ± 0.4°C) yielded resting CO2 production of 0.81 ± 0.06 ml · g−1 · h−1. Latency to the first electrical discharge was not affected by humidity. At 507-kPa O2, latency was 23 ± 0.4 and 22 ± 0.7 min in dry and humid conditions, respectively, and, at 608-kPa O2, latency was 15 ± 4 and 14 ± 3 min in dry and humid conditions, respectively. When no effects of CO2 and metabolic rate are present, humidity does not affect CNS oxygen toxicity. Relevance of the findings to diving and hyperbaric therapy is discussed.

Depletion of tissue glutathione with diethyl maleate enhances hyperbaric oxygen toxicity

1990 ◽  
Vol 258 (6) ◽  
pp. L308-L312 ◽  
Author(s):  
C. A. Weber ◽  
C. A. Duncan ◽  
M. J. Lyons ◽  
S. G. Jenkinson
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Hyperbaric Oxygen ◽  
Intraperitoneal Administration ◽  
Oxygen Toxicity ◽  
Lung Toxicity ◽  
Diethyl Maleate ◽  
Time To Death ◽  
Hyperbaric Hyperoxia ◽  
Hyperoxic Exposure

Rats exposed to hyperbaric hyperoxia experience severe central nervous system and lung toxicity. Exogenous glutathione administration has been shown to protect rats from the effects of hyperbaric hyperoxia. To explore the hypothesis that decreases in tissue glutathione (GSH) could increase the susceptibility of rats to hyperbaric hyperoxia, we administered diethyl maleate (DEM) (a compound that conjugates with GSH and rapidly lowers tissue levels) and measured tissue GSH levels. DEM administration decreased plasma GSH by 86%, liver GSH by 82%, and brain GSH by 45% between 2 and 4 h after injection with values returning to normal by 24 h. We then treated rats with DEM or saline and began exposure at 2 h after treatment to 100% oxygen at 4 ATA. Time-to-convulsion and time-to-death were recorded. Rats that received DEM 2 h before exposure seized earlier and died earlier than controls. Intraperitoneal administration of GSH to DEM-treated rats abolished the enhanced toxicity occurring during a hyperbaric hyperoxic exposure. DEM appears to increase the toxicity of rats exposed to hyperbaric hyperoxia by lowering tissue GSH levels, and replenishment of lung and brain GSH by exogenous administration reverses these effects.

scholarly journals HSP70 protects rats and hippocampal neurons from central nervous system oxygen toxicity by suppression of NO production and NF-κB activation

2018 ◽  
Vol 243 (9) ◽  
pp. 770-779 ◽  
Author(s):  
Hongjie Yi ◽  
Guoyang Huang ◽  
Kun Zhang ◽  
Shulin Liu ◽  
Weigang Xu
Keyword(s):  
Nitric Oxide ◽  
Central Nervous System ◽  
Nervous System ◽  
Heat Shock ◽  
Nitric Oxide Synthase ◽  
Heat Shock Protein ◽  
Hyperbaric Oxygen ◽  
Heat Shock Protein 70 ◽  
Oxygen Toxicity ◽  
Oxide Synthase

During diving, central nervous system oxygen toxicity may cause drowning or barotrauma, which has dramatically limited the working benefits of hyperbaric oxygen in underwater operations and clinical applications. The aim of this study is to understand the effects and the underlying mechanism of heat shock protein 70 on central nervous system oxygen toxicity and its mechanisms in vivo and in vitro. Rats were given geranylgeranylacetone (800 mg/kg) orally to induce hippocampal expression of heat shock protein 70 and then treated with hyperbaric oxygen. The time course of hippocampal heat shock protein 70 expression after geranylgeranylacetone administration was measured. Seizure latency and first electrical discharge were recorded to evaluate the effects of HSP70 on central nervous system oxygen toxicity. Effects of inhibitors of nitric oxide synthase and nuclear factor-κB on the seizure latencies and changes in nitric oxide, nitric oxide synthase, and nuclear factor-κB levels in the hippocampus tissues were examined. In cell experiments, hippocampal neurons were transfected with a virus vector carrying the heat shock protein 70 gene (H3445) before hyperbaric oxygen treatment. Cell viability, heat shock protein 70 expression, nitric oxide, nitric oxide synthase, and NF-κB levels in neurons were measured. The results showed that heat shock protein 70 expression significantly increased and peaked at 48 h after geranylgeranylacetone was given. Geranylgeranylacetone prolonged the first electrical discharge and seizure latencies, which was reversed by neuronal nitric oxide synthase, inducible nitric oxide synthase and NF-κB inhibitors. Nitric oxide, nitric oxide synthase, and inducible nitric oxide synthase levels in the hippocampus were significantly increased after hyperbaric oxygen exposure, but reversed by geranylgeranylacetone, while heat shock protein 70 inhibitor quercetin could inhibit this effect of geranylgeranylacetone. In the in vitro study, heat shock protein 70-overexpression decreased the nitric oxide, nitric oxide synthase, and inducible nitric oxide synthase levels as well as the cytoplasm/nucleus ratio of nuclear factor-κB and protected neurons from hyperbaric oxygen-induced cell injury. In conclusion, overexpression of heat shock protein 70 in hippocampal neurons may protect rats from central nervous system oxygen toxicity by suppression of neuronal nitric oxide synthase and inducible nitric oxide synthase-mediated nitric oxide production and translocation of nuclear factor-κB to nucleus. Impact statement Because the pathogenesis of central nervous system oxygen toxicity (CNS-OT) remains unclear, there are few interventions available. To develop an efficient strategy against CNS-OT, it is necessary to understand its pathogenesis and in particular, the relevant key factors involved. This study examined the protective effects of heat shock protein 70 (HSP70) on CNS-OT via in vivo and in vitro experiments. Our results indicated that overexpression of HSP70 in hippocampal neurons may protect rats from CNS-OT by suppression of nNOS and iNOS-mediated NO production and the activation of NF-κB. These findings contribute to clarification of the role of HSP70 in CNS-OT and provide us a potential novel target to prevent CNS-OT. Clarification of the involvement of NO, NOS and NF-κB provides new insights into the mechanism of CNS-OT and may help us to develop new approach against it by interfering these molecules.

Time-varying Spectral Index of Electrodermal Activity to Predict Central Nervous System Oxygen Toxicity Symptoms in Divers: Preliminary results

2021 ◽  
Author(s):  
Hugo F. Posada-Quintero ◽  
Bruce J. Derrick ◽  
Christopher Winstead-Derlega ◽  
Sara I. Gonzalez ◽  
M. Claire Ellis ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Spectral Index ◽  
Electrodermal Activity ◽  
Oxygen Toxicity ◽  
Time Varying ◽  
Preliminary Results

Glutamate metabolism of astrocytes during hyperbaric oxygen exposure and its effects on central nervous system oxygen toxicity

Neuroreport ◽  
2016 ◽  
Vol 27 (2) ◽  
pp. 73-79 ◽  
Author(s):  
Yu-Liang Chen ◽  
Dan Li ◽  
Zhong-Zhuang Wang ◽  
Wei-Gang Xu ◽  
Run-Ping Li ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Hyperbaric Oxygen ◽  
Oxygen Toxicity ◽  
Glutamate Metabolism ◽  
Oxygen Exposure ◽  
Hyperbaric Oxygen Exposure

Hyperoxic myopia: a case series of four divers

2020 ◽  
pp. 261-265
Author(s):  
Jonathan W. Brügger ◽  
Glenn A. Rauscher ◽  
John P. Florian ◽  
Keyword(s):  
Hyperbaric Oxygen ◽  
Prolonged Exposure ◽  
Case Series ◽  
Oxygen Toxicity ◽  
Hyperbaric Oxygen Treatment ◽  
Subjective Data ◽  
Residual Symptoms ◽  
Oxygen Treatment ◽  
Blurry Vision ◽  
Record Review

Hyperoxic myopia is a phenomenon reported in individuals who have prolonged exposure to an increased partial pressure of oxygen (PO2) and subsequently have a myopic (nearsighted) change in their vision. To date, there are numerous accounts of hyperoxic myopia in dry hyperbaric oxygen treatment patients; however, there have been only three confirmed cases reported in wet divers. This case series adds four confirmed cases of hyperoxic myopia in wet divers using 1.35 atmospheres (ATM) PO2 at the Navy Experimental Diving Unit (NEDU). The four divers involved were the first author’s patients at NEDU. Conditions for two divers were confirmed via record review, whereas the other two divers were diagnosed by the first author. All subjects were interviewed to correlate subjective data with objective findings. Each subject completed five consecutive six-hour hyperoxic (PO2 of 1.35 ATM) dives with 18-hour surface intervals. Each individual was within the U. S. Navy Dive Manual’s standards for general health. Visual acuity was measured prior to diving. Within three to four days after diving, the individuals reported blurry vision with an associated myopic refraction shift. Each diver had spontaneous resolution of his myopia over the next two to three weeks, with no significant residual symptoms. The divers in this case series were exposed to an increased PO2 (1.35 ATM for 30 hours over five days), a lesser exposure than that in other reports of hyperoxic myopia in wet divers diagnosed with hyperoxic myopia (1.3-1.6 ATM for 45-85 hours in 12-18 days). Furthermore, this pulse of exposure was more concentrated than typically seen with traditional hyperbaric oxygen therapy. Hyperoxic myopia continues to be a risk for those conducting intensive diving with a PO2 between 1.3-1.6 ATM. Additional investigation is warranted to better define risk factors and PO2 limits regarding ocular oxygen toxicity.

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